In the past, there was proposed an apparatus having an object for preventing atrial fibrillation from being induced by the increase of the heart rate in which vagus nerve (fat pad) is stimulated if the spontaneous heart rate exceeds a predetermined threshold (see, for example, PCT Jap. laid-open patent publication H7-504596 [lower right column of page 3]). This fat pad exists by accompanying a sino-atrial node or an atrioventricular node and the fat pad relating to the sino-atrial node exists at a bended entrance of a right pulmonary vein and is positioned along a ventral atrioventricular groove for most people. Also, the fat pad relating to the atrioventricular node is positioned at a bended coupling portion of a postcaval vein and a subordinate left atrium and is positioned along a dorsal atrioventricular groove for most people.
The apparatus described in the PCT Jap. laid-open patent publication H7-504596 T (lower right column of page 3) is a coupling pacemaker/fat pad stimulator which is to be implanted particularly in a patient who has atrial fibrillation or atrial flutter generating repetitively and who cannot receive sufficient procedure by a medical agent and it is constituted therein in order to sense occurrence of a rapid ventricle rate and to induce absolute or relative heart block such that a stimulation pulse for stimulating the fat pad accompanying the atrioventricular node is to be generated.
Then, the stimulation to the fat pad of the atrioventricular node induces the increase of the heart block, decreases ratio of atrium depolarization transmitted to the ventricle and slows down the ventricle rate. Consequently, the apparatus described in the Patent Reference 1 possesses an operation of a pacemaker which slows down heartbeat rate of the heart by the fat pad stimulation.
However, there is a case in which a serious heart damage occurs by other factors even in a case when the heart rate is not high. Particularly, for a patient who has an organic heart disease such as myocardial infarction, cardiomyopathy or the like, the degenerated, hypertrophied, fibrotic lesioned part and the peripheral part thereof of the myocardium and the endocardium become in an unstable state electrically and this electrical instability causes shortening of a refractory period, forming of an excitation reentry path accompanying thereof and accentuation of automaticity in the heart muscle or in an excitation conducting system or the like so as to make a fatal arrhythmia to occur easily. Consequently, there is a possibility in the apparatus described in the Patent Reference 1 that a fatal arrhythmia which cannot be prevented may occur.
In advance of the occurrence of the fatal arrhythmia, it has been recognized that occurrence of ventricular premature contraction, abnormality of ventricular repolarization process, change of electrogram ST potential or the like is caused and it has been considered such that all of them are important parameters as the precursor of the fatal arrhythmia. The ventricular premature contraction means a ventricular contraction which occurs earlier than timing predicted as a normal rhythm and if this triggers a reentry circuit formed in a heart muscle, ventricular tachycardia or ventricular fibrillation occurs due to reentry. Early afterdepolarization caused when repolarization of action potential of the heart muscle is damaged, delayed afterdepolarization in which depolarization of membrane potential is caused just after the end of repolarization or the like has been recognized for repolarization abnormality and it has been considered such that either one of those of depolarization has an occurrence mechanism of the ventricular tachycardia or the ventricular fibrillation by triggering a new excitation when the amplitude increases and reaches a threshold.
The ST change occurs by myocardial ischemia or myocardial infarction and an oxygen-deprived state of the heart muscle accompanying the myocardial ischemia or the myocardial infarction encourages electrical instability in which the fatal arrhythmia occurs easily. The electrical instability strongly receives influence of a functional factor such as an autonomic nerve or a heart rate and in particular, increase of the oxygen consumption of the heart muscle accompanying the heart rate increase or accentuation of the sympathetic nerve tension increases electrical instability which is primarily owned by a patient of an organic heart disease such as myocardial infarction, cardiomyopathy or the like and it makes a state for inducing a fatal arrhythmia easily by premature contraction, repolarization abnormality or ST change.